title: Time to positivity of a rapid bedside assay for cardiac-specific troponin T predicts prognosis in acute coronary syndromes: a Thrombolysis in Myocardial Infarction (TIMI) 11A substudy.
abstract: OBJECTIVE
  We sought to determine whether the rapid bedside assay for troponin T identified patients at risk for a more complicated hospital stay and a higher rate of adverse clinical events.
  
  
  BACKGROUND
  In patients with an acute coronary syndrome, the amount of cardiac-specific troponin T released bears a stoichiometric relation to the extent of myocardial damage.
  
  
  METHODS
  In 597 patients with unstable angina or non-Q wave myocardial infarction participating in the Thrombolysis in Myocardial Infarction (TIMI) 11A substudy, a rapid bedside assay and simultaneous quantitative serum measurement for troponin T were obtained at enrollment.
  
  
  RESULTS
  The composite end point of the sum of death, nonfatal myocardial infarction or recurrent ischemia through day 14 occurred in 33.6% of patients with a positive assay compared with only 22.5% of patients with a negative assay (p = 0.01). Those patients in whom the rapid assay became positive in < or = 10 min had the highest mortality rate of 4.2% through day 14 compared with 1.1% in those patients who had either a late-appearing positive assay (> 10 min) or a negative assay. The duration of hospital stay in the 116 patients (19%) with a positive rapid assay at enrollment was a median of 5 days compared with only 3 days in the 481 patients (81%) with a negative rapid assay at enrollment (p = 0.002).
  
  
  CONCLUSIONS
  A positive rapid assay for troponin T at presentation identifies those patients at risk for higher rates of adverse clinical events and longer, more complicated hospital stays. Stratification of patients by time to development of a positive rapid assay identifies those patients at highest mortality risk.
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. eantman@bustoff.bwh.harvard.edu
authors.forename: E M
authors.initials: EM
authors.lastname: Antman
authors.forename: D B
authors.initials: DB
authors.lastname: Sacks
authors.forename: N
authors.initials: N
authors.lastname: Rifai
authors.forename: C H
authors.initials: CH
authors.lastname: McCabe
authors.forename: C P
authors.initials: CP
authors.lastname: Cannon
authors.forename: E
authors.initials: E
authors.lastname: Braunwald
mesh_terms: D000368:Aged; D000789:Angina, Unstable / Q000097:blood* / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood; D002423:Cause of Death; D017984:Enoxaparin / Q000008:administration & dosage / Q000627:therapeutic use; D005260:Female; D005343:Fibrinolytic Agents / Q000008:administration & dosage / Q000627:therapeutic use; D005500:Follow-Up Studies; D005544:Forecasting; D006760:Hospitalization; D006801:Humans; D007902:Length of Stay; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy; D017202:Myocardial Ischemia / Q000097:blood / Q000209:etiology; D019095:Point-of-Care Systems; D011379:Prognosis; D012008:Recurrence; D012307:Risk Factors; D015996:Survival Rate; D013577:Syndrome; D015912:Thrombolytic Therapy; D013997:Time Factors; D014336:Troponin / Q000097:blood*; D020107:Troponin T
chemical_list: D015415:Biomarkers; D017984:Enoxaparin; D005343:Fibrinolytic Agents; D014336:Troponin; D020107:Troponin T